ArticleMolecular medicine reports2019
Curcumin inhibits high glucose‑induced inflammatory injury in human retinal pigment epithelial cells through the ROS‑PI3K/AKT/mTOR signaling pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
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- Natural antioxidant products and nanomaterial-based delivery systems for the amelioration of diabetic retinopathy: mechanisms, applications, and translational perspectives.Frontiers in immunology · 2026Review
- Influence of Certain Natural Bioactive Compounds on Glycemic Control: A Narrative Review.Nutrients · 2025Review
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- Curcuma Longa (turmeric): from traditional applications to modern plant medicine research hotspots.Chinese medicine · 2025Review
- Targeting mTOR with curcumin: therapeutic implications for complex diseases.Inflammopharmacology · 2025Review
- Isoegomaketone improves radiotherapy efficacy and intestinal injury by regulating apoptosis, autophagy and PI3K/AKT/mTOR signaling in a colon cancer model.Oncology reports · 2025Article
- Curcumin targets YAP1 to enhance mitochondrial function and autophagy, protecting against UVB-induced photodamage.Frontiers in immunology · 2025Article
- Study on the mechanism of plant metabolites to intervene oxidative stress in diabetic retinopathy.Frontiers in pharmacology · 2025Review
- Curcumin, an active component of turmeric: biological activities, nutritional aspects, immunological, bioavailability, and human health benefits - a comprehensive review.Frontiers in immunology · 2025Review
- On the health effects of curcumin and its derivatives.Food science & nutrition · 2024Review
- Nutraceuticals for Diabetic Retinopathy: Recent Advances and Novel Delivery Systems.Nutrients · 2024Review
- Healing effect of curcumin on tooth extraction sockets in diabetic rats.Journal of applied oral science : revista FOB · 2024Article
- Alcohol-induced liver injury in signalling pathways and curcumin's therapeutic potential.Toxicology reports · 2023Review
- Review
- Mechanistic insights into the alterations and regulation of the AKT signaling pathway in diabetic retinopathy.Cell death discovery · 2023Review
- The Effect of Adipose-Derived Mesenchymal Stem Cells on Peripheral Nerve Damage in a Rodent Model.Journal of clinical medicine · 2023Article
- New Insights on Dietary Polyphenols for the Management of Oxidative Stress and Neuroinflammation in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2023Review
- Substance P Alleviates Retinal Pigment Epithelium Dysfunction Caused by High Glucose-Induced Stress.Life (Basel, Switzerland) · 2023Article
- The signaling pathways of traditional Chinese medicine in treating diabetic retinopathy.Frontiers in pharmacology · 2023Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) is a retinal disease caused by metabolic disorders of glucose tolerance that can lead to irreversible blindness if not adequately treated. Retinal pigment epithelial cell (RPEC) dysfunction contributes to the pathogenesis of DR. In the present study the anti‑inflammatory effect of curcumin (CUR) was investigated in RPECs damaged by high glucose levels. RPEC treated with 30 mmol/l glucose was regarded as high glucose group, and cells treated with 24.4 mmol/l mannitol was set as equivalent osmolarity group. Cell Counting Kit‑8 assay was used to measure RPEC viability, the expression of phosphorylated (p)‑AKT and p‑mammalian target of rapamycin (mTOR) were assessed by western blot, and secretion of tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and IL‑1β in the culture medium was measured by ELISA. Intracellular reactive oxygen species (ROS) levels were measured by laser scanning confocal microscope. The present data indicated that, compared with mannitol treatment, high glucose treatment reduced RPEC viability, increased TNF‑α, IL‑6 and IL‑1β secretion, increased ROS formation and promoted phosphorylation of AKT and mTOR. The antioxidant N‑acetylcysteine, the phosphoinositide 3‑kinase (PI3K)/AKT inhibitor LY294002 and the mTOR inhibitor rapamycin ameliorated the effects of high glucose. In addition, pretreatment with 10 µmol/l CUR reduced secretion levels of TNF‑α, IL‑6 and IL‑1β, ROS formation and phosphorylation of AKT and mTOR. In conclusion, CUR inhibited high glucose‑induced inflammatory injury in RPECs by interfering with the ROS/PI3K/AKT/mTOR signaling pathway. The present study may reveal the molecular mechanism of CUR inhibition effects to high glucose‑induced inflammatory injury in RPEC.
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